Function of the Heart
- Functions via calcium binding to troponin, which causes tropomysin to move and exposes myosin binding sites on the actin filament, allowing ATP mediated contraction to occur
Figure 1: The Cardiac Troponin-Actin-Myosin Complex
- The function of the heart can be described by Pressure-Volume Loops which consist of 2 curves: End Systolic Pressure Volume Relationship (ESPVR) and End Diastolic Pressure Volume Relationship (EDPVR)
- ESPVR is analogous to the Frank-Starling relationship which describes increasing force generated by a muscle fiber when stretched. Hence, surrogate measures can be used for "stretch" such as preload, end diastolic pressure, or end diastolic volume while surrogate measures can be used for "force" such as stroke volume, cardiac output, etc.
- Changes in inotropy shift the ESPVR curve left with increases in inotropy and rightwards with decreases in inotropy (Figure 3)
- Changes in lusitropy, or the compliance/diastolic function/ability of the heart to relax, shift the EDPVR curve, rightwards with increased compliance (ie with Milrinone) or leftwards with decreasing compliance (Figure 4)
Figure 2: The LV Pressure and Volume curves over time (left) as well as the LV Pressure/Volume Loop
Figure 3: Starling Curves Figure 4: LV Diastolic Curve Figure 5: Putting the Two Together
Interpreting the CVP waveform
Figure 6: The CVP Waveform
The normal CVP waveform (Figure 6) consists of various waves:
1) a wave: due to atrial contraction at the end of diastole
2) c wave: due to the tricuspid valve bulging into the RA during isovolumic contraction
3) x descent: due to atrial relaxation as the ventricle contracts
4) v wave: due to filling of the atrium during systole
5) y descent: due to emptying of the atria into the ventricle during diastole
Various pathological processes can alter the CVP waveform:
1) canon a waves: large a waves seen with AV dissociation (ie JET) as the atrium contracts against a closed tricuspid valve
2) loss of a waves: occurs in atrial fibrillation as there is no longer a significant atrial contraction
3) prominent CV wave: occurs with tricuspid regurgitation; as the ventricle contracts, the regurgitation causes an increase in the C and V waves
Figure 7: Pressure, Volume EKG, Heart Sounds over the Cardiac Cycle
Treatment of Hemodynamic Dysfunction
Fundamentally, Ohm's Law states: Voltage= Current X Resistance. This can be applied to hemodynamics in that: Change in pressure = Flow X Resistance.
Hence, for systemic hemodynamics:
Systemic blood pressure = CO X Systemic Vascular Resistance (SVR)
CO= HR X SV
For any state of hypotension, it is either an issue with cardiac output and/or systemic vascular resistance. Typically, the body will compensate for the perturbation by increasing the other component.
For example:
1) Decreased cardiac output (ie cardiogenic shock, hypovolemia, bradyarrythmia, etc), the body compensates for low CO by increasing SVR to try and maintain BP. Hence, the patient looks clamped down with poor peripheral perfusion and capillary refill. This is COLD SHOCK. You want to augment cardiac output in this situation (via fluid for increased preload, inotropy for poor contractility, chronotropy for bradyarrhythmias, etc) and perhaps even reduce SVR (decrease afterload) on the stressed heart. The patient is already vasoconstricted and so vasopressor agents that further SVR are less useful in this circumstance (and perhaps even harmful).
2) Decreased SVR (ie anaphylaxis, distributive shock), the body compensates for low SVR by increasing CO. Hence, the patient is hyperdynamic, has flash capillary refill and bounding pulses. This is WARM SHOCK. You want to use agents (ie norepinephrine) that will increase SVR. The patient is likely already hyperdynamic so inotropic (B1) agents are less useful in this circumstance.
- Treatment consists of treating the underlying etiology (bleeding, hypovolemia, sepsis, etc)
- Fluids are given for augmenting preload to take advantage of the Frank-Starling relationship
- Vasoactive agents are used to augment SVR or cardiac output, depending on the pathophysiology (see below)
Figure 8: Common Vasoactives and Their Effects
